Altered bacterial metabolism, not coenzyme Q content, is responsible for the lifespan extension in Caenorhabditis elegans fed an Escherichia coli diet lacking coenzyme Q

Abstract

SummaryCoenzyme Q n is a fully substituted benzoquinone containing a polyisoprene tail of distinct numbers (n) of isoprene groups. Caenorhabditis elegans fed Escherichia coli devoid of Q 8 have a significant lifespan extension when compared to C. elegans fed a standard 'Q-replete' E. coli diet. Here we examine possible mechanisms for the lifespan extension caused by the Q-less E. coli diet. A bioassay for Q uptake shows that a water-soluble formulation of Q 10 is effectively taken up by both clk-1 mutant and wild-type nematodes, but does not reverse lifespan extension mediated by the Q-less E. coli diet, indicating that lifespan extension is not due to the absence of dietary Q per se. The enhanced longevity mediated by the Q-less E. coli diet cannot be attributed to dietary restriction, different Qn isoforms, reduced pathogenesis or slowed growth of the Q-less E. coli , and in fact requires E. coli viability. Q-less E. coli have defects in respiratory metabolism. C. elegans fed Q-replete E. coli mutants with similarly impaired respiratory metabolism due to defects in complex V also show a pronounced lifespan extension, although not as dramatic as those fed the respiratory deficient Q-less E. coli diet. The data suggest that feeding respiratory incompetent E. coli , whether Q-less or Q-replete, produces a robust life extension in wild-type C. elegans . We believe that the fermentation-based metabolism of the E. coli diet is an important parameter of C. elegans longevity.

Microbial Genetic Composition Tunes Host Longevity

“…This molecule is a biochemical precursor for many aromatic metabolites (Bentley, 1990). Synthetic deficiencies in two of the chorismate derivatives, ubiquinone and folate, underlie the prolonged host lifespan by the E. coli mutants previously identified (Saiki et al, 2008; Virk et al, 2012). A life-prolonging drug metformin exerts its beneficial effects by interfering with bacterial methionine biosynthesis, which is also coupled with chorismate metabolism (Cabreiro et al, 2013).…”

Gut microbiota as a candidate for lifespan extension: an ecological/evolutionary perspective targeted on living organisms as metaorganisms

“…Animals grown on heat-or UV-killed OP50 bacteria live longer than those fed live bacteria (Garigan et al 2002). In laboratory settings, different components of the worm diet (Collins et al 2006;Yang et al 2009), different sources of non-pathogenic bacterial food (Reinke et al 2010), and of bacterial constituents (Lenaerts et al 2008;Saiki et al 2008) can modulate worm longevity. Different forms of dietary restriction were shown to increase C. elegans lifespan impinging on common and unique longevity-regulatory pathways (Greer and Brunet 2009).…”

Promoting Health and Longevity through Diet: From Model Organisms to Humans

“…Feeding C. elegans with soil bacteria, Bacillus mycoides and Bacillus soli , instead of the standard laboratory E. coli OP50 strain, significantly extends lifespan and stress resistance, suggesting that microbial-derived factors may play modulate pro-longevity pathways (Abada et al 2009). Moreover, wild-type C. elegans fed respiratory incompetent E. coli show increased lifespan (Saiki et al 2008). A comparison of the effects of E. coli and Comamonas aquatica on the C. elegans host identified vitamin B12 as a major diffusable factor from Comamonas that influenced patterns of gene expression and the rate of development and fertility of the worm (Watson et al, 2014).…”